Moderate exercise is an antioxidant: Upregulation of antioxidant genes by training

Gómez-Cabrera, Mari Carmen; Doménech, Elena; Viña, José

doi:10.1016/j.freeradbiomed.2007.02.001

Cited by 825 publications

(715 citation statements)

References 52 publications

Supporting

Mentioning

642

Contrasting

Unclassified

Order By: Relevance

“…We have found that skeletal muscle from aged and KO PGC-1α animals exhibit oxidative stress, i.e., an increase in protein carbonylation, in resting conditions. The protein oxidation was not significantly increased after training in any experimental group which is in accordance with our idea that exercise training does not increase oxidative stress (Gomez-Cabrera et al 2008b). Previous work from our laboratory as well as from others has demonstrated that interfering with free radical production with antioxidants may hamper mitochondriogenic activation by exercise (GomezCabrera et al 2008a;Strobel et al 2010;Ristow et al 2009).…”

Section: Discussionsupporting

confidence: 91%

“…We provided the first clearcut evidence that exercise generates oxidative stress only when it is exhaustive (Sastre et al 1992;GomezCabrera et al 2003). However, physical exercise can be considered as a double edge sword: when practiced strenuously it causes oxidative stress and cell damage but when practiced with moderation, it increases the expression of antioxidant enzymes and thus should be considered as an antioxidant (Gomez-Cabrera et al 2008b). Here, we have measured the effect of exercise training on skeletal muscle protein oxidation status in young and aged rats and in WT and PGC-1α KO mice.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Age associated low mitochondrial biogenesis may be explained by lack of response of PGC-1α to exercise training

Derbré

Gómez-Cabrera

Nascimento

et al. 2011

AGE

Self Cite

114

View full text Add to dashboard Cite

Low mitochondriogenesis is critical to explain loss of muscle function in aging and in the development of frailty. The aim of this work was to explain the mechanism by which mitochondriogenesis is decreased in aging and to determine to which extent it may be prevented by exercise training. We used aged rats and compared them with peroxisome proliferator-activated receptor-γ coactivator-1α deleted mice (PGC-1α KO). PGC-1α KO mice showed a significant decrease in the mitochondriogenic pathway in muscle. In aged rats, we found a loss of exercise-induced expression of PGC-1α, nuclear respiratory factor-1 (NRF-1), and of cytochrome C. Thus muscle mitochondriogenesis, which is activated by exercise training in young animals, is not in aged or PGC-1α KO ones. Other stimuli to increase PGC-1α synthesis apart from exercise training, namely cold induction or thyroid hormone treatment, were effective in young rats but not in aged ones. To sum up, the low mitochondrial biogenesis associated with aging may be due to the lack of response of PGC-1α to different stimuli. Aged rats behave as PGC-1α KO mice. Results reported here highlight the role of PGC-1α in the loss of mitochondriogenesis associated with aging and point to this important transcriptional coactivator as a target for pharmacological interventions to prevent age-associated sarcopenia.

show abstract

Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Age associated low mitochondrial biogenesis may be explained by lack of response of PGC-1α to exercise training

Derbré

Gómez-Cabrera

Nascimento

et al. 2011

AGE

Self Cite

114

View full text Add to dashboard Cite

show abstract

“…(PhSe) 2 was prepared in our laboratory according to the literature method. 23 Analysis of the 1 H NMR and 13 C NMR spectra showed that (PhSe) 2 obtained presented analytical and spectroscopic data in full agreement with its assigned structure.…”

Section: Chemicalsmentioning

confidence: 99%

“…However, there is increasing evidence that RONS not only are toxic but also play an important role in cell signaling and in the regulation of gene expression. 2 During strenuous exercise, there is a dramatic increase in oxygen uptake in various organs, particularly in the skeletal muscle. 3 Studies have demonstrated that delayed-onset muscle damage is mainly induced by mechanical stress, especially peculiar muscle contraction.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Antioxidant effect of diphenyl diselenide on oxidative stress caused by acute physical exercise in skeletal muscle and lungs of mice

Prigol

Luchese

Nogueira

2009

Cell Biochemistry & Function

View full text Add to dashboard Cite

This study was designed to examine if diphenyl diselenide (PhSe) 2 , an organoselenium compound, attenuates oxidative stress caused by acute physical exercise in skeletal muscle and lungs of mice. Swiss mice were pre-treated with (PhSe) 2 (5 mg kg -1 day -1 ) for 7 days. At the 7th day, the animals were submitted to acute physical exercise which consisted of continuous swimming for 20 min. The animals were euthanized 1 and 24 h after the exercise test. The levels of thiobarbituric acid reactive species (TBARS), non-protein thiols (NPSH) and ascorbic acid and the activity of catalase (CAT) were measured in the lungs and skeletal muscle of mice. Glycogen content was determined in the skeletal muscle of mice. Parameters in plasma (urea and creatinine) were determined. The results demonstrated an increase in TBARS levels induced by acute physical exercise in the skeletal muscle and lungs of mice. Animals submitted to exercise showed an increase in non-enzymatic antioxidant defenses (NPSH and ascorbic acid) in the skeletal muscle. In lungs of mice, activity of CAT was increased. (PhSe) 2 protected against the increase in TBARS levels and ameliorated antioxidant defenses in the skeletal muscle and lungs of mice submitted to physical exercise. These results indicate that acute physical exercise caused a tissue-specific oxidative stress in the skeletal muscle and lungs of mice. (PhSe) 2 protected against oxidative damage induced by acute physical exercise in mice.

show abstract

Embracing complexity of (brain) aging

Polidori

2024

FEBS Letters

View full text Add to dashboard Cite

Aging is a multifactorial process occurring in a pathophysiological continuum which leads to organ and system functional loss. While aging is not a disease, its pathophysiological continuum predisposes to illness and multimorbidity clusters which share common biomolecular mechanisms—the pillars of aging. Brain aging and neurodegeneration share many hallmarks with other age‐related diseases. The central nervous system is often the weakest link susceptible to the aging process and its deterioration, resulting in cognitive impairment and other symptoms; the aging process is associated with proteostasis collapse, stem cell exhaustion, repair mechanisms, altered brain nutrient sensing, endothelial changes, inflammation, oxidative distress, and energy unbalance, as well as other disturbances. These mechanisms are highly interwoven, and considerable research is aimed at their disentanglement and detection of their clinically relevant impact, particularly in order to identify pharmacological and non‐pharmacological preventive and therapeutic strategies.

show abstract

Moderate exercise is an antioxidant: Upregulation of antioxidant genes by training

Cited by 825 publications

References 52 publications

Age associated low mitochondrial biogenesis may be explained by lack of response of PGC-1α to exercise training

Age associated low mitochondrial biogenesis may be explained by lack of response of PGC-1α to exercise training

Antioxidant effect of diphenyl diselenide on oxidative stress caused by acute physical exercise in skeletal muscle and lungs of mice

Embracing complexity of (brain) aging

Contact Info

Product

Resources

About